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. 2019 Aug 23;42(5):1781–1792. doi: 10.3892/or.2019.7293

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Copyright: © Zhuang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — Co-culture with MSCs^Hypoxia induces modulation of the TGF-β1/Smad signaling pathway. Representative images of western blots of (A and B) Smad7 and β-actin expression and (C and D) p-Smad3 and Smad3 from fibroblasts, fibroblasts treated with radiation, and fibroblasts co-cultured with MSCs^Hypoxia or MSCs^Hypoxia + anti-HGF antibody or recombinant TGF-β1. Each column represents the mean ± SD from three independent experiments; ^*P<0.05 vs. the Control; ^▲P<0.05 vs. Radiation + MSCs^Hypoxia. (E and F) Fibroblasts were transfected with siRNA-Smad7, or with siRNA-NT as a control. siRNA-mediated transfection efficiency was determined by western blotting. Each column represents the mean ± SD from three independent experiments; ^*P<0.05 vs. siRNA-Smad7. MSCs, mesenchymal stem cells; HGF, hepatocyte growth factor.